McLachlan D R
Neurobiol Aging. 1986 Nov-Dec;7(6):525-32. doi: 10.1016/0197-4580(86)90102-8.
There is now substantial evidence indicating that an accumulation of aluminum occurs in grey matter in diseases associated with Alzheimer neurofibrillary degeneration. Four principle sites of aluminum accumulation have been identified in Alzheimer's disease: DNA containing structures of the nucleus, the protein moieties of neurofibrillary tangles, the amyloid cores of senile plaques and cerebral ferritin. Consideration of the extensive information now available on the toxic effects of aluminum in these four loci strengthens the hypothesis that aluminum could be important in the pathogenesis of this neurodegenerative process. The evidence, however, does not support an etiological role for aluminum in Alzheimer's disease. The primary pathogenic events responsible for Alzheimer's disease are presumed to have affected the genetically determined barriers to aluminum resulting in increased amounts of this toxic element to vulnerable target sites.
现在有大量证据表明，在与阿尔茨海默病神经纤维变性相关的疾病中，灰质中会出现铝的蓄积。在阿尔茨海默病中已确定铝蓄积的四个主要部位：细胞核中含DNA的结构、神经纤维缠结的蛋白质部分、老年斑的淀粉样核心和脑铁蛋白。考虑到目前可获得的关于铝在这四个位点的毒性作用的大量信息，强化了铝在这种神经退行性过程的发病机制中可能起重要作用的假说。然而，证据并不支持铝在阿尔茨海默病中的病因学作用。推测导致阿尔茨海默病的主要致病事件影响了对铝的遗传决定屏障，导致这种有毒元素在易损靶位点的量增加。
